Up-regulation of sarcoplasmic reticulum Ca2+ uptake leads to cardiac hypertrophy, contractile dysfunction and early mortality in mice deficient in CASQ2 | Zendy

Anuradha Kalyanasundaram | Zendy; Véronique A. Lacombe | Zendy; Andriy E. Belevych | Zendy; Lucia Brunello | Zendy; Cynthia A. Carnes | Zendy; Paul M.L. Janssen | Zendy; Björn C. Knollmann | Zendy; Muthu Periasamy | Zendy; Sándor Györke | Zendy

Open Access

Up-regulation of sarcoplasmic reticulum Ca2+ uptake leads to cardiac hypertrophy, contractile dysfunction and early mortality in mice deficient in CASQ2

Author(s) -

Anuradha Kalyanasundaram,

Véronique A. Lacombe,

Andriy E. Belevych,

Lucia Brunello,

Cynthia A. Carnes,

Paul M.L. Janssen,

Björn C. Knollmann,

Muthu Periasamy,

Sándor Györke

Publication year - 2012

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1093/cvr/cvs334

Subject(s) - calsequestrin , phospholamban , ryanodine receptor , medicine , serca , ryanodine receptor 2 , endocrinology , heart failure , myocyte , endoplasmic reticulum , biology , muscle hypertrophy , calcium , microbiology and biotechnology , atpase , biochemistry , enzyme

Although aberrant Ca(2+) release (i.e. Ca(2+) 'leak') from the sarcoplasmic reticulum (SR) through cardiac ryanodine receptors (RyR2) is linked to heart failure (HF), it remains unknown whether and under what conditions SR-derived Ca(2+) can actually cause HF. We tested the hypothesis that combining dysregulated RyR2 function with facilitated Ca(2+) uptake into SR will exacerbate abnormal SR Ca(2+) release and induce HF. We also examined the mechanisms for these alterations.

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